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uric acid/inflammation
Врската е зачувана во таблата со исечоци
Страница 1 од 2518 резултати
The peroxynitrite scavenger uric acid prevents inflammatory cell invasion into the central nervous system in experimental allergic encephalomyelitis through maintenance of blood-central nervous system barrier integrity.
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Uric acid (UA), a product of purine metabolism, is a known scavenger of peroxynitrite (ONOO(-)), which has been implicated in the pathogenesis of multiple sclerosis and experimental allergic encephalomyelitis (EAE). To determine whether the known therapeutic action of UA in EAE is mediated through
Elevated serum uric acid is associated with vascular inflammation but not coronary artery calcification in the healthy octogenarians: the Brazilian study on healthy aging.
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BACKGROUND
There is a limited data on the association between serum uric acid (SUA) and cardiovascular disease (CVD) among the very elderly population.
OBJECTIVE
We evaluated the association of SUA, highly sensitive C-reactive protein (hs-CRP, a marker of vascular and systemic inflammation), and
Plasmodium-induced inflammation by uric acid.
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Infection of erythrocytes with the Plasmodium parasite causes the pathologies associated with malaria, which result in at least one million deaths annually. The rupture of infected erythrocytes triggers an inflammatory response, which is induced by parasite-derived factors that still are not fully
Effect of nonsteroidal anti-inflammatory drugs on the renal excretion of uric acid.
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The effect of 9 nonsteroidal anti-inflammatory drugs on the renal excretion of uric acid was studied in patients with normal renal function. Diflunisal, Azapropazone and Indomethacin caused an increase and Piroxicam a decrease in the uric acid excretion. Other drugs studied had no significant
Pro-inflammatory effects of uric acid in the gastrointestinal tract.
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Uric acid can be generated in the gastrointestinal (GI) tract from the breakdown of nucleotides ingested in the diet or from purines released from host cells as a result of pathogen-induced cell damage. Xanthine oxidase (XO) is the enzyme that converts hypoxanthine or xanthine into uric acid, a
Inflammatory response of uric acid produced by Porphyromonas gingivalis gingipains
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Uric acid is a potential metabolite that serves as a danger-associated molecular pattern and induces inflammatory responses in sterile environments. Porphyromonas gingivalis is a keystone periodontopathogen, and its gingipain proteases play a critical role in the pathogenesis of periodontitis. In
Conversion of Th17-type into Th2-type inflammation by acetyl salicylic acid via the adenosine and uric acid pathway in the lung.
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BACKGROUND
Allergen-specific T-cell responses orchestrate airway inflammation, which is a characteristic of asthma. Recent evidence suggests that noneosinophilic asthma can be developed by mixed Th1 and Th17 cell responses when exposed to lipopolysaccharide (LPS)-containing allergens.
OBJECTIVE
To
Uric acid in chronic heart failure: a marker of chronic inflammation.
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BACKGROUND
Chronic heart failure is associated with hyperuricaemia and elevations in circulating markers of inflammation. Activation of xanthine oxidase, through free radical release, causes leukocyte and endothelial cell activation. Associations could therefore be expected between serum uric acid
Uric acid correlates to oxidation and inflammation in opposite directions in women.
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OBJECTIVE
To evaluate the association of uric acid (UA) levels with a panel of markers of oxidative stress and inflammation.
METHODS
Plasma UA levels, along with a panel of oxidative stress and inflammatory markers, were measured in 755 Chinese women.
RESULTS
Plasma UA levels were inversely
Long non-coding RNA ANRIL-mediated inflammation response is involved in protective effect of rhein in uric acid nephropathy rats.
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The xanthine oxidase inhibitor Febuxostat reduces tissue uric acid content and inhibits injury-induced inflammation in the liver and lung.
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Necrotic cell death in vivo induces a robust neutrophilic inflammatory response and the resulting inflammation can cause further tissue damage and disease. Dying cells induce this inflammation by releasing pro-inflammatory intracellular components, one of which is uric acid. Cells contain high
Adiponectin protects against uric acid‑induced renal tubular epithelial inflammatory responses via the AdipoR1/AMPK signaling pathway.
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Adiponectin (APN) exerts anti‑inflammatory effects in various cells. Uric acid (UA) induces inflammation in proximal renal tubular epithelial cells (PTECs). It remains unknown whether APN protects against UA‑induced inflammation. In the present study, human PTECs were incubated with 100 µg/ml
Sex-related association of serum uric acid with inflammation, kidney function and blood pressure in type 1 diabetic patients.
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OBJECTIVE
Recent studies suggest that uric acid (UA) is a mediator of diabetic nephropathy. We hypothesized that serum UA would associate with the prevalence of diabetic nephropathy in youth with type 1 diabetes (T1D), and that this relationship would differ by sex.
METHODS
We examined 120 young
The association of renal tubular inflammatory and injury markers with uric acid excretion in chronic kidney disease patients.
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Pro-inflammatory and oxidative effects of noncrystalline uric acid in human mesangial cells: contribution to hyperuricemic glomerular damage.
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Hyperuricemia is associated with cardiovascular and renal diseases, as glomerulosclerosis. Noncrystalline uric acid induces deleterious effects on endothelial and vascular smooth muscle cells. In the present study, we analyzed the damage induced by UA on human mesangial cells (HMC), the potential
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